COVID Seattle: cardic probs

thought i would circulate this. from a person on the blog list (not wanting to be credited). this is from seattle, and is about 3 weeks old. i expect Boston will be at level of seattle pretty soon....

this was after my blog on myocarditis, and the cardiac items were highlighted.

geoff

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“We've been told not to share info, but we are all doing it anyway.

Since COVID is now deemed endemic in the XXXX area, and to quote a reliable source, the rest of the country is just "lagging behind," thought I'd share some relevant details, including from CDC teleconference today for COVID providers.

- as we all assumed, it has been in community spread locally for weeks. We have seen idiopathic ARDS cases since early/mid-Feb. Retrospective testing is being done where possible. - the numbers presented in media do not reflect actual cases, obvs. Testing here only started 2/28. Our first CONFIRMED death was 2/23.

=XXX State Lab can only run 26kits/day, though they are ramping up quickly. Despite strict criteria for testing, there is a 3d backlog at this time.

- Negative Resp Path PCR is required before SARS2 test will be accepted. We have been running out of RP PCRs. This is unheard of, especially as most admitted resp pts get one during flu/cold season (mostly for approp iso, since RSV is contact). Goddess bless the local Children's hospital for sending us 60 the other night. Your hospital should begin stocking up on RP PCRs now. Our Public Health dept does not expect SARS2 tests to be ample enough to d/c the neg RP PCR requirement.

- on a related note, county lab no longer runs tests from pts not sick enough to be admitted, since dz is now endemic. Expect this will be the case elsewhere soon.

- as of today, we have 21 pts and 11 deaths since 2/28. Not including the postmortem retrospective dx of pts who died with idiopathic ARDS the prior week. Of note, Harborview had an idiopath ARDS death 2/26. There will be more retrospective dx. - our mortality rate is skewed up (and in some cases, down) because many of our pts come from the LCCK SNF (Lifecare Care Center of Kirkland) & are elderly and severely chronically medically ill - the sort of pts who die of rhinovirus. Many of these patients' families are opting for comfort care, as many are DNI. We have 3 such on the floor on comfort care now. Of note, those 3 pts have what would be considered mild infxn in a different cohort.

- we are seeing pts who are young (20s), fit, no comorbidities, critically ill. It does happen. - media (including NYT) are mentioning "efforts to contain the outbreak" at the SNF.

I'm sure you are all aware, but the US has been past containment since January, and the SNF cases aren't an "outbreak" they're a cluster. - thus far many pts have contacts there (esp visiting family members), but also at a local HD center and a car dealership. Others have zero identifiable contacts at all, tho I suspect many have Costco-horde connections, heh. - fortunately Evergreen has capability to turn all or half of any ward into a neg pressure zone

Currently, all of ICU is for critically ill COVIDs, all of XXX floor medsurg for stable COVIDs and EOL care, half of PCU, half of ER. New resp-sx pts Pulmonary Clinic offshoot is open.

- in XXXX, CDC is no longer imposing home quarantine on providers who were wearing only droplet iso PPE when intubating, suctioning, bronching, and in one case doing bloody neurosurgery on these pts in the week prior to testing starting. Because that resulted in our Stroke Center hospital no longer being able to admit LVOs or any kind of bleed. And decimated 10% of our Hospitalists, 3 of the 6 Night docs, and a PCCM. Plus it's now endemic. Expect when it comes to your place you may initially have staff home-quarantined. Plan for this NOW. Consider wearing airborne iso PPE for aerosol-generating procedures in ANY pt in whom you suspect COVID, just to prevent the mass quarantines.

- we ran out of N95s (thanks, Costco hoarders) and are bleaching and re-using PAPRs, which is not the manufacturer's recommendation. Not surprised on N95s as we use mostly CAPRs anyway, but still. Supplies are en route, but your facility may wish to stock up now, esp if you expect each staff member and room to have its own PAPR/CAPR.

- terminal cleans (inc UV light) for ER COVID rooms are taking forever, Enviro Services is overwhelmed. Bad as pts are stuck coughing in the waiting room. Rec planning now for Enviro upstaffing, or having a plan for sick pts to wait in their cars (that is not legal here, sadly).

- CLINICAL INFO based on our cases and info from CDC conf call today with other COVID providers in US:

- the Chinese data on 80% mildly ill, 14% hospital-ill, 6-8% critically ill are generally on the mark. Data very skewed by late and very limited testing, and the number of our elderly pts going to comfort care.

 - being young & healthy (zero medical problems) does not rule out becoming vented or dead - probably the time course to developing significant lower resp sx is about a week or longer (which also fits with timing of sick cases we started seeing here, after we all assumed it was endemic as of late Jan/early Feb).

 - based on our hospitalized cases (including the not formally diagnosed ones who are obviously COVID - it is quite clinically unique) about 1/3 have mild lower resp sx, need 1-5L NC. 1/3 are sicker, FM or NRB. 1/3 tubed with ARDS. Thus far, everyone is seeing: - nl WBC. Almost always lymphopenic, occasionally poly-predominant but with nl total WBC. Doesn't change, even 10days in.

 - BAL lymphocytic despite blood lymphopenic (try not to bronch these pts; this data is from pre-testing time when we had several idiopathic ARDS cases)
- fevers, often high, may be intermittent; persistently febrile, often for >10d. It isn't the dexmed, it's the SARS2.

 - low ProCalc; may be useful to check initially for later trending if later concern for VAP etc. - up AST/ALT, sometimes alk phos. Usually in 70-100 range. No fulminant hepatitis. Notably, in our small sample, higher transaminitis at admit (150-200) correlates with clinical deterioration and progression to ARDS. LFTs typically begin to bump in 2nd week of clinical course. - mild AKI (Cr <2). Uncertain if direct viral effect, but notably SARS2 RNA fragments have been identified in liver, kidneys, heart, and blood.

- characteristic CXR always bilateral patchy or reticular infiltrates, sometimes perihilar despite nl EF and volume down at presentation. At time of presentation may be subtle, but always present, even in our pts on chronic high dose steroids. NO effusions. CT is as expected, rarely mild mediastinal LAD, occ small effusions late in course which might be related to volume status/cap leak.

- Note - China is CT'ing everyone, even outpts, as a primarily diagnostic modality. However, in US/Europe, CT is rare, since findings are nonspecific, would not change management, and the ENTIRE scanner and room have to terminal-cleaned, which is just impossible in a busy hospital. Also, transport in PAPRs. Etc. 2 of our pts had CTs for idiopathic ARDS in the pre-test era; they looked like the CTs in the journal articles. Not more helpful than CXR. - when resp failure occurs, it is RAPID (likely 7-10d out from sx onset, but rapid progression from hospital admit). 

Common scenario for our pts is, admit 1L NC. Next 12hrs -> NPPV. Next 12-24hrs -> vent/proned/Flolan. - interestingly, despite some needing Flolan, the hypoxia is not as refractory as with H1N1. Quite different, and quite unique. Odd enough that you'd notice and say hmmm. - thus far many are dying of cardiac arrest rather than inability to ventilate/oxygenate. - given the inevitable rapid progression to ETT once resp decompensation begins, we and other hosps, including Wuhan, are doing early intubation. Facemask is fine, but if needing HFNC or NPPV just tube them. They definitely will need a tube anyway, & no point risking the aerosols. - no MOSF. There's the mild AST/ALT elevation, maybe a small Cr bump, but no florid failure. except cardiomyopathy. 

- multiple pts here have had nl EF on formal Echo or POCUS at time of admit (or in a couple of cases EF 40ish, chronically). Also nl Tpn from ED. Then they get the horrible resp failure, sans sepsis or shock. Then they turn the corner, off Flolan, supined, vent weaning, looking good, never any pressor requirement. Then over 12hrs, newly cold, clamped, multiple-pressor shock that looks cardiogenic, EF 10% or less, then either VT->VF-> dead or PEA-> asystole in less than a day. Needless to say this is awful for families who had started to have hope. 

- We have actually had more asystole than VT, other facilities report more VT/VF, but same time course, a few days or a week after admit, around the time they're turning the corner. This occurs on med-surg pts too; one today who is elderly and chronically ill but baseline EF preserved, newly hypoTN overnight, EF<10. Already no escalation, has since passed, So presumably there is a viral CM aspect, which presents later in the course of dz. - of note, no WMAs on Echo, RV preserved, Tpns don't bump. Could be unrelated, but I've never seen anything like it before, esp in a pt who had been HD stable without sepsis.

Treatment -

- Remdesivir might work, some hosps have seen improvement with it quite rapidly, marked improvement in 1-3 days. ARDS trajectory is impressive with it, pts improve much more rapidly than expected in usual ARDS.

- Recommended course is 10d, but due to scarcity all hosps have stopped it when pt clinically out of the woods - none have continued >5d. It might cause LFT bump, but interestingly seem to bump (200s-ish) for a day or 2 after starting then rapidly back to normal - suggests not a primary toxic hepatitis.

- unfortunately, the Gilead compassionate use and trial programs require AST/ALT <5x normal, which is pretty much almost no actual COVID pts. Also CrCl>30, which is fine. CDC is working with Gilead to get LFT reqs changed now that we know this is a mild viral hepatitis.

-currently the Gilead trial is wrapping up, NIH trial still enrolling, some new trial soon to begin can't remember where.

- steroids are up in the air. In China usual clinical practice for all ARDS is high dose methylpred. Thus, ALL of their pts have had high dose methylpred. Some question whether this practice increases mortality.

- it is likely that it increases seconday VAP/HAP. China has had a high rate of drug resistant GNR HAP/VAP and fungal pna in these pts, with resulting increases mortality. We have seen none, even in the earlier pts who were vented for >10d before being bronched (prior to test availability, again it is not a great idea to bronch these pts now).

- unclear whether VAP-prevention strategies are also different, but wouldn't think so?

- Hong Kong is currently running an uncontrolled trial of HC 100IV Q8.

- general consensus here (in US among docs who have cared for COVID pts) is that steroids will do more harm than good, unless needed for other indications.

- many of our pts have COPD on ICS. Current consensus at Evergreen, after some observation & some clinical judgment, is to stop ICS if able, based on known data with other viral pneumonias and increased susceptibility to HAP. Thus far pts are tolerating that, no major issues with ventilating them that can't be managed with vent changes. We also have quite a few on AE-COPD/asthma doses of methylpred, so will be interesting to see how they do.

That's all I got for now. Will be skipping the next 2 CDC COVID calls as working Nights, but will call in again next week and keep you all posted.

Plz share info but preferably with no direct attribution as I need to remain employed"  

On Wed, Mar 25, 2020 at 11:36 AM Geoff A. Modest, M.D. <GModest@uphams.org> wrote:

I have heard of a few cases of myocarditis associated with the SARS-CoV-2, one from a physician in Kansas reporting on a COVID-positive patient with respiratory distress, atypical chest pain, EKG changes suggestive of a STEMI but clean (ie atherosclerosis-free) coronary arteries; and an LA cardiologist responding that she has been seeing myocarditis-like presentations.

There is little written about this that i could find, but a case report from China was published in the European Society of Cardiology journal, describing a patient with fulminant myocarditis associated with coronavirus who apparently responded to glucocorticoids and human immunoglobulin (see covid myocarditis eurjcard2020 in dropbox, or doi:10.1093/eurheartj/ehaa190).

Case:

-- 37-year-old male admitted to the hospital with chest pain and dyspnea for 3 days, and diarrhea.

-- Blood pressure 80/50

-- Troponin-T was >10,000 ng/L; CK-MB 112.9 ng/L;  BNP was 21,025 ng/L

-- chest x-ray found cardiac enlargement. Chest CT showed pulmonary infection, enlarged heart, and pleural effusion. EKG showed ST elevation consistent with acute MI (leads 3, AVF). Emergent CT coronary angiogram showed no coronary stenosis.

-- Echo showed a large heart with ejection fraction 27%; left atrium 39 mm, right ventricle 25 mm, right atrium 48 mm, 2 mm of pericardial effusion

-- sputum was examined for 13 respiratory viruses: only coronavirus positive. negative for: influenzas A (including H1N1 and H3N2) and B, Mycoplasma pneumoniae, adenovirus, bocavirus, rhinovirus, parainfluenza, chlamydia, and RSV

-- clinical diagnosis was coronavirus fulminant myocarditis with cardiogenic shock and pulmonary infection

Therapy:

-- methylprednisolone 200 mg per day for 4 days to suppress inflammation

-- immunoglobulin 20 g per day for 4 days to regulate immune status

-- norepinephrine to raise blood pressure

-- diuretics (torsemide and furosemide)

-- milrinone to increase myocardial contractility

-- piperacillin sulbactam for infection

-- pantoprazole

-- with above, symptoms improved significantly. Chest x-ray one week later showed normal size heart, echo showed size and function of the heart had returned to normal, with LVEF 66%

-- troponin-T decreased to 220.5, CK MB to 9, BNP to 1587

-- by 3 weeks all of the myocardial injury markers had fully normalized

Commentary:-- I bring this up just because myocarditis may be an important and serious complication of coronavirus, as it is with many different viral infections. And some of the clinical presentation for myocarditis may be incorrectly attributed to the more common ARDS or some other severe pulmonary complications. And though this was only one patient, their results are intriguing, should be studied more rigorously, and the therapy they used may be an option for a severely ill person with fulminant myocarditis

-- they did not check for many of the other common viral etiologies of myocarditis. in the setting of China (or other more endemic coronavirus areas), for a person with myocarditis, and with evaluation finding a positive coronavirus and negative flu and several other infections, the putative role of the coronavirus is pretty likely

-- however, they did not definitively confirm myocarditis (no cardiac MRI, endomyocardial biopsy), though clinically seems very likely

--  the role of steroids is not so clear even in ARDS, with observational trials on both sides:

    -- a study finding that steroids may be harmful, and not recommending their use (see covid steroids not likely help lancet2020 in dropbox, or doi.org/10.1016/ S0140-6736(20)30317-2), and another finding twice the mortality in those on steroids (see covid mortality risk factors lancet2020, or doi.org/10.1016/S0140-6736(20)30566-3)

     -- but another study finding a 60% lower death rate with steroids (see covid steroids help ards jamaintmed2020 in dropbox, or doi:10.1001/jamainternmed.2020.0994)

-- a longer term issue: though it is important to figure out the best treatment regimen for the acute situation, it is also unclear what the long-term consequences of this viral myocarditis will be (ie, is this likely to progress to a dilated cardiomyopathy?)

--so, the big issue here is that most of what we are doing is in an evidence-free zone. we really need good RCTs to guide us. 

    -- for example: in the above observational steroid studies, were those put on steroids sicker (ie, doing poorly so they tried everything?), or perhaps they were they less sick (more hope for recovery in a situation where people are being triaged for therapies/care being rationed??? and mostly giving up on the sickest ones??).

    -- should we even try the combination of steroids/immunoglobulins in a patient who seems to be dying of fulminant myocarditis?? that may be reasonable, but we really don't know if that person may have recovered spontaneously and in fact the steroids did nothing or may even have been harmful. 

    -- and maybe they did not have myocarditis by more specific testing (though this was a pretty likely diagnosis). and was it the steroids, the immunoglobulin, or both that was potentially beneficial.

but i thought it was useful to put myocarditis on our radar screens as a possible complication of SARS-CoV-2 infection

geoff​

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